Anterior chamber associated immune deviation (ACAID) is a phenomenon that has been well described in the mouse eye. With ACAID, antigens placed into the anterior chamber (AC) are presented to the host immune system in such a way that delayed-type hypersensitivity (DTH) responses are suppressed. ACAID may be an important factor contributing to the "immune privilege of the eye". Furthermore, exploration of the ACAID phenomenon is of importance to our understanding of transplantation biology, immune regulation, chronic inflammatory conditions and possibly the immune resistance to intraocular tumors and pathogens. Presumably, antigen presenting cells (APCs) are present in the AC that mediate suppression of DTH. In addition, factors have been identified in aqueous fluid that suppress antigen-driven lymphocyte proliferation. However, the precise mechanism of ACAID is unknown as is the location of the APCs. APCs express Class II MHC surface antigens. We have found that human and mouse trabecular cells express these antigens constitutively. We speculate that as part of the aqueous outflow system, the trabecular meshwork may be involved in antigen presentation and thereby influence immune responses in the AC. The goals of this study are to more precisely characterize the Class II antigen-bearing cells in the aqueous outflow system and to further explore the relationship between the outflow channels and ACAID. The nature of the Class II positive cells in the human outflow system will be analyzed using immunofluorescence and immunoelectron microscopy. The number of positive cells will be quantitated and correlated with age. The effect of Class II expression on other trabecular cell functions will be explored. The ability of human trabecular cells to suppress antigen-driven lymphocyte proliferation will be studied. Parallel studies will be performed in an inbred mouse model. Immunoelectron microscopy will be used to characterize the Ia-positive cells. The origin of these cells will be explored with bone marrow chimera studies. We will refine our experimental model of glaucoma in the mouse and rat eye and use this model to explore the importance of aqueous drainage to the development of ACAID.